Published online May 26, 2014. doi: 10.4330/wjc.v6.i5.314
Revised: February 5, 2014
Accepted: March 17, 2014
Published online: May 26, 2014
Processing time: 178 Days and 19.6 Hours
Immune-driven inflammation plays an important part in atherogenesis and is therefore believed to be key to the development of cardiovascular disease (CVD), which is currently the leading cause of death in the Western world. By fulfilling some of the Koch postulates, atherogenesis has even been proposed to be considered as an autoimmune disease, raising the hope that CVD could be prevented by immunomodulation. Nevertheless, the role of the immune system and autoimmune reactions in atherosclerosis appear to be a double edged-sword, with both pro-atherogenic and anti-atherogenic attributes. Hence, if immunomodulation is to become a therapeutic option for atherosclerosis and CVD, it will be crucial to correctly identify patients who might benefit from targeted suppression of deleterious autoimmune responses. This could be achieved, for example, by the detection of disease-associated autoantibodies. In this work, we will review the currently available clinical, in vitro, and animal studies dedicated to autoantibodies against apolipoprotein A-1 (anti-apoA-1 IgG), the major proteic fraction of high density lipoprotein. Current clinical studies indicate that high levels of anti-apoA-1 IgG are associated with a worse cardiovascular prognosis. In addition, in vitro and animal studies indicate a pro-inflammatory and pro-atherogenic role, supporting the hypothesis that these autoantibodies may play a direct causal role in CVD, and furthermore that they could potentially represent a therapeutic target for CVD in the future.
Core tip: This review provides a comprehensive and critical analysis of the most recent basic research articles and clinical trials on the role of autoantibodies to apolipoprotein A-1 as biomarkers and potential mediators of cardiovascular diseases (CVD). Evidence from both in vitro and in vivo studies showed that anti-apolipoprotein A-1 IgG might have critical pro-atherosclerotic activities by activating immune cells to release pro-inflammatory mediators and proteases. In addition, these autoantibodies might increase heart rate and arrhythmias both in humans and animal models. These studies suggest a causal role of anti-apolipoprotein A-1 immunoglobulins of G class in CVD, indicating that those autoantibodies could potentially represent an emerging therapeutic target to better fight CVD.